A mechanism study on propofol's action on middle latency auditory evoked potential by neurons in ventral partition of medial geniculate body in rats.
A mechanism study on propofol's action on middle latency auditory evoked potential by neurons in ventral partition of medial geniculate body in rats.
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发表时间：
2014-07
影响因子：
3.3
通讯作者：
Qiqing Shi;X. Sun;H. Fang
中科院分区：
文献类型：
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作者：
Qiqing Shi;X. Sun;H. Fang
目的 探讨异丙酚对大鼠内侧膝状体腹侧区（MGBv）神经元中潜伏期听觉诱发电位（MLAEP）的影响并探讨其作用机制。材料与方法 SD大鼠随机分为7组（n = 6）：生理盐水组（NS）、脂肪乳组（I）和不同浓度异丙酚组（5.6、16.8、56、168、560 µmol/L）（P1-P5）。这些动物用乙醚麻醉、气管切开并机械通气。麻醉后，用维库溴铵使大鼠麻痹并固定。通过立体定向将装有药物的记录针电极插入 MGBv 中。注射 0.2 µl 异丙酚、生理盐水或脂肪乳后，通过 MLAEP 对标准声音的响应来验证正确插入。记录 MLAEP，包括 N0、P0、Na、Pa 和 Nb 波的幅度和潜伏期。为了确定异丙酚可能影响哪些离子通道，将SD大鼠分为Ni2++异丙酚（A1组）、Cd2++异丙酚（A2组）、4-AP+异丙酚（A3组）和TTX+异丙酚（A4组）。记录注射4种离子通道阻滞剂和异丙酚之间MLAEP的变化。使用全细胞膜片钳技术来确认这些变化。结果NS、I、P1、P2组给药后MGBv各波MLAEP与注射前基线比较均无明显变化。 P3、P4、P5组注射后Na、Pa、Nb波潜伏期较基线显着延长，Pa波幅值较基线降低。 P3、P4和P5组Na、Pa和Nb波的潜伏期显着更长，Pa波的振幅显着低于NS和I组。使用TTX时，Na-Pa波的振幅降低。给予丙泊酚后，Na-Pa 中的波没有变化，Na、Pa 和 Nb 中的潜伏期增加。对于 Cd2+，Na、Pa 和 Nb 中的潜伏期没有变化，而 Na-Pa 中的振幅降低。然而，给予Ni2+和4-AP后，每波MLAEP均无变化。注射异丙酚后，Na-Pa 波振幅减小，Na、Pa 和 Nb 波潜伏期增加。膜片钳结果显示，56μmol/L、168μmol/L和560μmol/L异丙酚对大鼠脑片的持续钠电流和高压活化钙电流有抑制作用。结论 56 µmol/L、168 µmol/L和560 µmol/L异丙酚可抑制大鼠MGBv中MLAEP，且呈剂量依赖性，这种变化可能是通过阻断持续钠电流和高压激活钙电流的离子通道引起的。
OBJECTIVES To investigate the effect of propofol on the middle latency auditory evoked potentials (MLAEP) by neurons in the ventral partition of medial geniculate body (MGBv) in rats and study their mechanism. MATERIALS AND METHODS Sprague-Dawley (SD) rats were randomly divided into 7 groups (n = 6): group normal saline (NS), group intralipid (I), and groups of different concentrations of propofol (5.6, 16.8, 56, 168, 560 µmol/L) (P1-P5). These animals were anesthetized with ether, tracheostomized, and mechanically ventilated. After anesthesia, rats were paralyzed with vecuronium and fixed. A recording needle electrode with drugs was inserted into MGBv by means of stereotaxis. After injection of 0.2 µl propofol, normal saline or intralipid, correct insertion was verified by MLAEP response to standard sound. MLAEP including amplitudes and latencies of N0, P0, Na, Pa, and Nb waves were recorded. To identify which ion channel could be impacted by propofol, SD rats were divided into Ni2+ plus propofol (A1 group), Cd2+ plus propofol (A2 group), 4-AP plus propofol (A3 grouop), and TTX plus propofol (A4 group). The changes of MLAEP were recorded between injecting 4 ion channel blockers and propofol. Whole-cell patch clamp technique was used to confirm these variations. RESULTS There was no significant changes in all waves of MLAEP in MGBv after drug administration as compared with the baselins before injection in group NS, I, P1, and P2. The latency of Na, Pa, and Nb wave was significantly prolonged and the amplitude of Pa wave was decreased after injection as compared with the baseline in group P3, P4, and P5. The latency of Na, Pa, and Nb waves was significantly longer and the amplitude of Pa wave was significantly lower in group P3, P4, and P5 than in group NS and I. With TTX, amplitudes were decreased in wave Na-Pa. After given propofol, waves were unchanged in Na-Pa and latency was increased in Na, Pa, and Nb. With Cd2+, latency was unchanged in Na, Pa, and Nb as well as amplitudes decreasing in Na-Pa. Nevertheless, after given Ni2+ and 4-AP, every wave of MLAEP had no changes. After injected propofol, amplitudes were decreased in wave Na-Pa and latency was increased in Na, Pa, and Nb. The results of patch clamp showed 56 µmol/L, 168 µmol/L and 560 µmol/L propofol inhibited the persistent sodium currents and high voltaged activated calcium currents in the brain slices of rats. CONCLUSIONS Propofol in 56 µmol/L, 168 µmol/L and 560 µmol/L can inhibit MLAEP in MGBv of rats in a dose-dependent manner and these changes may be caused by blocking the ion channel of persistent sodium currents and high voltaged activated calcium currents.